Ventricular Fibrillation and Ventricular Tachycardia Triggered by Late‐Coupled Ventricular Extrasystoles in a Brugada Syndrome Patient

Premature ventricular complexes (PVC) falling after the end of the T wave triggered ventricular fibrillation (VF) at night and monomorphic ventricular tachycardia (MVT) during daytime, in a recipient of implantable cardioverter defibrillator with Brugada syndrome. Treatment with bepridil (1) decreased the height of ST segment elevation in leads V1‐V3, (2) completely eliminated VF, and (3) markedly decreased the incidence of PVC and MVT. Albeit rare, VF can be triggered by late‐coupled PVC, due to a mechanism other than phase 2 reentry in some patients with Brugada syndrome. (PACE 2011; e1–e5)     

Ventricular Fibrillation Triggered during and after Radiofrequency Energy Delivery to the Site of Origin of Idiopathic Right Ventricular Outflow Tract Arrhythmia

We observed a case of idiopathic ventricular arrhythmias originating from the right ventricular outflow tract (RVOT). The origin of target premature ventricular contraction (PVC) and nonsustained ventricular tachycardia (VT) was within a wide low‐voltage area around the RVOT. During radiofrequency (RF) application to the site of arrhythmia origin, polymorphic VT and ventricular fibrillation were repeatedly triggered by new PVC that had developed near the site of ablation. This electrical storm persisted >30 minutes after cessation of RF current delivery, and was suppressed by additional RF applications to the site of origin of the new PVC.     

Spontaneous Deterioration of Atrioventricular Nodal Reentrant Tachycardia to Polymorphic Ventricular Tachycardia in the Absence of Heart Disease

Atrioventricular nodal reentrant tachycardia (AVNRT) is usually associated with a good prognosis. This is a case of a 57‐year woman who presented with supraventricular tachycardia that spontaneously deteriorated to polymorphic ventricular tachycardia (PVT). The PVT terminated without treatment after 16 seconds. Extensive cardiac evaluation including echocardiography, stress testing, coronary angiography, and cardiac magnetic resonance imaging did not reveal any structural heart disease. Electrophysiology testing demonstrated typical AVNRT which was successfully treated with cryoablation. The clinical ventricular tachycardia could not be reproduced despite the use of an aggressive induction protocol and isoproterenol. Postablation, exercise treadmill testing did not provoke any tachyarrhythmia. The patient is doing well 13 months later. In summary, we present the rare finding of a moderately fast, typical AVNRT degenerating to a long run of PVT, in the absence of any detectable heart disease or other etiology for PVT. (PACE 2011; 34:e14–e17)     

Successful Catheter Ablation of Focal Ventricular Fibrillation in a Patient with Nonischemic Dilated Cardiomyopathy

A 64‐year‐old man with nonischemic dilated cardiomyopathy and a biventricular defibrillator presented with recurrent ventricular fibrillation (VF) and defibrillator shocks. Evaluation of the intracardiac electrograms from his defibrillator demonstrated the consistent initiation of VF by unifocal premature ventricular complexes (PVCs). Noncontact mapping demonstrated the origin of the PVC to be near the left ventricular outflow tract toward the mitral valve ring. Several applications of radiofrequency at this position led to complete cessation of PVCs and prevented further VF. He has not had any further ventricular arrhythmias or defibrillator discharges during follow‐up. (PACE 2011; 34:e38–e42)     

Myocardial contrast echocardiography (MCE) with triggered ultrasound does not cause premature ventricular complexes: evidence from PB127 MCE studies.

Previous studies suggest that myocardial contrast echocardiography using high mechanical index triggered ultrasound can be associated with increased frequency of the premature ventricular complex (PVC). However, this association has not been systematically examined. PB127 (Point Biomedical Corp, San Carlos, Calif) is a novel microsphere designed for evaluation of myocardial perfusion with ultrasound. PB127 myocardial contrast echocardiography was performed with triggered harmonic power Doppler in early/mid diastole (mechanical index .999) and was lower than untriggered intervals (P =.001) in B, suggesting that triggers do not cause PVC. PB127 does not cause increase PVC frequency during or after imaging with triggered ultrasound at mechanical index of 1.     

Tp‐e and (Tp‐e)/QT ratio as a non‐invasive risk factors for malignant ventricular arrhythmia in patients with idiopathic ventricular premature complexes

BackgroundTo evaluate the role of Tp‐e and (Tp‐e)/QT ratio in differentiating benign ventricular premature complex (VPC) and malignant polymorphic ventricular tachycardia (PVT).MethodsFrom January 2017 to December 2017, patients with documented polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) were consecutive included and classified as PVT/VF group. Sixty age‐ and sex‐matched healthy individuals were recruited as comparative control and subdivided into non‐VPC and VPC group. Clinical characteristics and Tp‐e and Tp‐e/QT ratio between the three groups were compared.ResultsTp‐e and (Tp‐e)/QT ratio were significantly higher in patients of PVT/VF group compared with the other two groups (P < .001). Episodes of syncope were more frequent in patients with PVT/VF (P < .05). The sensitivity and specificity of a Tp‐e interval ≥86 ms for malignant arrhythmias triggered by VPCs were 88% and 66%, respectively, while the sensitivity and specificity of the Tp‐e/QT ratio ≥0.24 were 82% and 70%, respectively. Five patients complained recurrence of syncope in the PVT/VF group and 1 patient died with mean follow‐up of 18 months.ConclusionTp‐e interval and the Tp‐Te/QT ratio is significantly increased in patients with PVT/VF and may be used as a novel non‐invasive marker of differentiating malignant and benign VPC.     

Evidence for an Intramural Origin of Idiopathic Premature Ventricular Contractions Successfully Ablated within the Great Cardiac Vein

A 37‐year‐old woman with idiopathic premature ventricular contractions (PVCs), exhibiting a right bundle branch block and inferior axis QRS morphology, underwent electrophysiological testing. The earliest ventricular activation with an isolated prepotential was observed within the great cardiac vein during the PVCs. Pacing from this site with an output of 10 mA produced an excellent pace map, whereas that with an output of 2 mA produced a wider QRS with notches in the early phase. A radiofrequency application delivered at this site eliminated the PVCs. These findings suggested that the PVC origin might have been intramural rather than epicardial. (PACE 2011; 34:e112–e114)     

Late gadolinium enhancement CMR in patients with tachycardia-induced cardiomyopathy caused by idiopathic ventricular arrhythmias

Background: Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia‐induced cardiomyopathy (TICMP). The aim of this study was to determine the prevalence of late gadolinium enhancement (LGE) in patients with TICMP caused by idiopathic ventricular arrhythmias. Methods: The study population consisted of 298 consecutive patients (174 F/124 M; mean age 45 ± 17 years) with frequent PVCs and/or VT. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF ≥15% after effective treatment of index ventricular arrhythmia. Results: Twenty‐seven (9.1%) patients found to have LVEF ≤50% and diagnosed as presumptive TICMP. Improvement in LVEF after effective treatment of index ventricular arrhythmia was observed in 22 of 27 patients (TICMP group; mean PVC burden of 30.8 ± 9.9%). LVEF did not improve in five of 27 patients (primary cardiomyopathy group; mean PVC burden of 28.8 ± 10.1%). LGE‐cardiac magnetic resonance (CMR) imaging was performed in 19 of 22 patients with TICMP and one patient (5%) had LGE. All five patients with primary cardiomyopathy underwent LGE‐CMR imaging and four patients (80%) had LGE. Conclusions: LGE is a rare finding in patients with TICMP caused by idiopathic ventricular arrhythmias. LGE‐CMR can be used in the diagnostic work‐up of patients with TICMP. Further prospective studies are required to determine the role of LGE‐CMR in predicting the recovery of left ventricular systolic dysfunction in patients with presumptive TICMP. PACE 2012; 35:465–470)     

Differentiation of Arrhythmias in the Dog by Measurement of Activation Sequence Using an Atrial and Two Ventricular Electrodes

Timing of atrioventricular activation and ventricular dispersion identifies and discriminates between beats of different origin. In eight dogs, three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during arrhythmias induced by programmed electrical stimulation and coronary artery occlusion and release. The interval between the left atrial and left ventricular intrinsic deflections (V₁-V₂) and between the left ventricular and right ventricular intrinsic deflections (V₁-V₂) of each heat was measured. Recordings were of normal sinus rhythm (NSR) (mean of five beats in 8/8 dogs), atrial flutter (AFL) (five beats of one episode), atrial fibrillation (AF) (144 beats in 29 episodes in 7/8), monomorphic ventricular tachycardia (MVT) (24 beats with six morphologies in 2/8), polymorphic ventricular tachycardia (PVT) (63 beats in 15 episodes in 5/8) and premature ventricular contractions (PVC) (29 beats with 29 morphologies in 5/8). Supraventricular rhythms can be differentiated from ventricular rhythms by V₁-V₂ timing. The mean difference in V₁-V₂ during AFL and AF vs NSR was 1 ms (range of 0–3 ms). The change from sinus during MVT ranged from 38 to 43 ms (m 31 ms) and during PVC 10 to 75 ms (m 38 ms). Thirty-five of 35 of these ectopic ventricular morphologies exhibited 10 ms or more timing difference compared to corresponding beats of NSR. PVT was consistently distinguished from supraventricular rhythms and MVT by the variability of V₁-V₂,A-V₁ intervals can be used to distinguish supraventricular arrhythmias from sinus rhythm; a 32 ms difference existed for AFL. AF could be detected by the variability in AV₁. One atrial and two ventricular leads can provide a means of differentiating normal sinus rhythm from supraventricular and ventricular arrhythmias that may be applicable to implantable antitachycardia devices.     

Calcium-Triggered Short-Coupled Polymorphous Ventricular Tachycardia

We describe a case of an 18-year-old man presenting with syncope found to have short-coupled premature ventricular complexes (PVCs) with subsequent nonsustained polymorphous ventricular tachycardia (PVT). Electrophysiology testing revealed premature PVCs and PVT provoked by calcium but not isoproterenol. It was noted that the earliest triggered event appeared to arise from ventricular muscle with subsequent involvement of the fascicles and these areas were ablated. The potential mechanisms for calcium triggering of these arrhythmias are discussed. (PACE 2010; 33:117–122)     

Long‐term follow‐up of patients with portal vein thrombosis and myeloproliferative neoplasms

Summary. Background: Myeloproliferative neoplasms (MPNs) are frequently identified as an underlying cause in patients with non‐cirrhotic portal vein thrombosis (PVT). The aim of this study was to describe the long‐term outcome of patients with PVT and MPN. Methods: A cohort study was performed including all adult patients referred to our hospital between 1980 and 2008 with non‐cirrhotic, non‐malignant PVT and confirmed MPN. Results: A total of 44 patients (70% female) were included, with a median age at PVT‐diagnosis of 48 years (range 18–79). In 31 patients (70%) PVT was the first manifestation of an MPN. Additional risk factors for thrombosis were present in 20 patients (45%). Median follow‐up was 5.8 years (range 0.4–21). Twenty‐three patients (52%) were treated with oral anticoagulants after diagnosis of PVT, of whom 15 (34%) received long‐term therapy. During follow‐up, 17 patients (39%) experienced at least one episode of gastrointestinal bleeding. Additional thrombotic events occurred in 12 patients (27%). Twelve patients (27%) had progression of the underlying MPN. Seventeen patients (39%) died at a median age of 64 years (range 30–88). Death was directly related to end‐stage MPN in eight patients (47%) and to a new thrombotic event in three patients (18%). No patients died from gastrointestinal bleeding. Conclusions: PVT is often the presenting symptom of an underlying MPN, highlighting the need for thorough screening for this disease. Recurrent thrombosis is a common and severe complication in patients with PVT and MPN. Mortality is primarily related to the underlying MPN and not to complications of portal hypertension.     

Pregnancy and Short‐Coupled Torsades de Pointes

This 24‐year‐old woman had incessant polymorphic ventricular tachycardia (PVT) during week 24 of her pregnancy and received over 200 implantable cardioverter‐defibrillator discharges. She failed to respond to quinidine, magnesium, isoproterenol, amiodarone, esmolol, and cilostazol during her PVT storm, although her dramatic response to verapamil was consistent with the diagnosis of short‐coupled variant of torsades de pointes. The case illustrated the utility of extracorporeal membrane oxygenation during refractory PVT, while attempting diagnostic and therapeutic pharmacologic maneuvers.     

Premature ventricular contractions during triggered imaging with ultrasound contrast.

BACKGROUND: Premature ventricular contractions (PVCs) were observed during triggered second harmonic imaging of a contrast agent for myocardial perfusion assessment, with continuous infusion of the contrast agent. Further investigation into the relation of this phenomenon to both ultrasound energy and the contrast agent was carried out during a subsequent bolus-versus-infusion study. METHODS AND RESULTS: Two open-label studies in healthy male volunteers were performed. The initial study was a dose-response study in 10 subjects, which compared 3 infusion rates. Each volunteer received 3 continuous infusions with different infusion rates of the contrast agent for either 10 (n = 6) or 20 (n = 4) minutes. End-systolic triggered imaging with a mechanical index (MI) of 1.5 was used throughout this part of the study. The second study compared bolus injection with a continuous infusion in 9 volunteers, with a single-dose level but different imaging modalities: end-systolic and end-diastolic triggered imaging at MIs of both 1.1 and 1.5. Spontaneous baseline PVCs were uncommon: 10 in 344 minutes (0.03 PVC/min, maximal 1 PVC/min) of baseline imaging. During end-diastolic triggering, no increase in PVCs was seen, irrespective of MI. A significant increase to 1.06 PVC/min (P <.001) was seen during end-systolic imaging with an MI of 1.5, but not with an MI of 1.1. The increase in PVC rate was dose-dependent in the initial study. CONCLUSION: Imaging of contrast agents with high acoustic pressures can cause PVCs if end-systolic triggering is used. This effect is related to both the dose of contrast agent and acoustic pressure. It does not occur during end-diastolic triggered imaging. Precautionary measures would include using lower MIs or end-diastolic triggering.     

An Acute Myocardial Infarction Case that Survived An Out‐of‐Hospital Cardiac Arrest in Which Prominent Ischemic J Waves Were Documented

We describe a case of a myocardial infarction, in which prominent ischemic J waves were documented during recurrent ventricular fibrillation attacks. The patient was referred to our hospital to treat an out‐of hospital cardiac arrest. Although the 12‐lead electrocardiogram obtained just after the first cardioversion did not show any apparent J waves, a J wave‐like steep downsloping type ST‐segment elevation associated with q waves in the inferior leads was documented during multiple episodes of ventricular fibrillation. Our report revealed the appearance of J waves as an important marker for lethal arrhythmias in acute ischemia. (PACE 2012; 35:e27–e30)     

Linking as the Cause of Unnecessary Right Ventricular Pacing

Background: The current report describes a manifestation of linking phenomenon in DDD pacemaker recipients: impairment of atrioventricular (AV) conduction and ensuing unnecessary right ventricular (RV) pacing. Methods: Three patients with second‐degree AV block and sudden impairment of native AV conduction following pacemaker implantation are presented. Loss of native AV conduction was considered functional and related to repetitive retrograde invasion of ventricular depolarization to the AV junction that was “linked” to ventricular pacing triggered by nonconducted P‐waves. Conclusion: This case series demonstrates that linking phenomenon should be considered in analysis of pacemaker behavior, and that retrograde concealment can be responsible for unnecessary RV pacing. (PACE 2010; 1359–1363)     

Prognostic role of high-sensitivity C-reactive protein and B-type natriuretic peptide in implantable cardioverter-defibrillator patients

Background: High‐sensitivity C‐reactive protein (hs‐CRP) and B‐type natriuretic peptide (BNP) are useful biomarkers for cardiovascular risk stratification. Little data are available regarding the prognostic value of hs‐CRP and BNP serum levels and future ventricular arrhythmic events triggering implantable cardioverter defibrillator (ICD) therapy. Methods: A total of 100 patients eligible for ICD implantation were enrolled in a prospective cohort study. Serum levels of hs‐CRP and BNP were obtained the day before ICD implantation and at scheduled follow‐up visits. For risk analysis, the study cohort was dichotomized based on serum level of hs‐CRP using a cut‐off value of 3 mg/L. The endpoint was appropriate ICD therapy triggered by ventricular arrhythmias during a follow‐up of 24 months. Results: Appropriate ICD therapy was delivered in 20% of patients. Median baseline serum level of hs‐CRP was significantly higher in patients with appropriate ICD therapy than in those without appropriate ICD therapy (5.33 mg/L vs 2.19 mg/L; P = 0.002). The same was true for median serum levels of hs‐CRP and BNP during follow‐up (5.43 mg/L vs 2.61 mg/L, P = 0.001 and 261.0 pg/mL vs 80.1 pg/mL, P = 0.01, respectively). Multivariate analysis demonstrated that baseline hs‐CRP level > 3 mg/L was independently associated with appropriate ICD therapy (odds ratio 4.0, 95% 1.1–14.2; P = 0.03). Conclusion: Elevated preimplantation hs‐CRP serum level is independently associated with increased risk for appropriate ICD therapy. Monitoring for elevated BNP levels during follow‐up adds to the assessment of risk for future arrhythmias. (PACE 2011;1–8)     

Role of Left Ventricular Scar and Purkinje‐Like Potentials During Mapping and Ablation of Ventricular Fibrillation in Dilated Cardiomyopathy

Background: Purkinje‐like potentials (PLPs) have been described as important contributors to initiation of ventricular fibrillation (VF) in patients with normal hearts, ischemic cardiomyopathy, and early after‐myocardial infarction. Methods: Of the 11 consecutive patients with VF storm, nonischemic cardiomyopathy (68 ± 22 years, left ventricular ejection fraction 28 ± 8%) who were given antiarrhythmic drugs and/or heart failure management, five had recurrent VF and underwent electrophysiology study (EPS) and catheter ablation. Results: At EPS, frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia did not occur. With isoproterenol, VF was induced in three patients, and sustained monomorphic PVCs were induced in one patient. Three‐dimensional electroanatomical mapping using CARTO (Biosense‐Webster Inc., Diamond Bar, CA) revealed posterior wall scar in four of the five patients. PLP in sinus rhythm were recorded around the scar border in these four patients, and radiofrequency ablation targeting PLP was successfully performed at these sites. The patient without PLP did not undergo ablation. During follow‐up (12 ± 5 months), only the patient without PLP had four VF recurrences requiring implantable cardioverter‐defibrillator (ICD) shocks. Conclusion: In patients with VF and dilated cardiomyopathy, left ventricular posterior wall scar in the vicinity of the mitral annulus seems to be a common finding. Targeting PLP along the scar border zone for ablation seems to efficiently prevent VF recurrence in these patients.     

Noncontact Mapping Guided Ablation of Right Ventricular Outflow Tract Ectopy in a Patient with Interruption of the Inferior Vena Cava and Azygos Continuation

A 58‐year‐old woman with symptomatic multiple monomorphic premature ventricular beats of a right ventricular outflow tract origin was referred for ablation. An inferior vena cava interruption with azygos continuation was discovered during catheter placement. This case describes positioning of the noncontact mapping array and successful radiofrequency ablation in this challenging anatomy. (PACE 2013; 36:e129–e131)     

Magnesium Sensitive,Adenosine Resistant,Repetitive Monomorphic Ventricular Tachycardia

Repetitive monomorphic ventricular tachycardia (RMVT) is characterized by episodes of ventricular ectopy and nonsustained VT exacerbated by catecholamines. Because this arrhythmia is frequently adenosine sensitive, its mechanism is believed to be cyclic adenosine monophosphate‐mediated triggered activity due to delayed afterdepolarizations. We present a case of RMVT associated with significant hypomagnesemia (serum level = 1.1 mg/dL), which did not respond to intravenous (IV) adenosine and terminated repeatedly after IV magnesium. Electrophysiologic study demonstrated an origin from the left sinus of Valsalva, which was successfully ablated. The combination of adenosine resistance and magnesium sensitivity may be consistent with an atypical RMVT mechanism related to inhibition of sodium‐potassium adenosine triphosphatase (Na⁺‐K⁺ ATPase).     

Idiopathic Ventricular Tachycardia Originating from the Left Ventricle Near the His Bundle

A 62‐year‐old man with idiopathic ventricular tachycardia (VT) exhibiting left bundle branch block and left inferior axis QRS morphology with a Qr in lead III underwent electrophysiological testing. Successful ablation was achieved in the left ventricle (LV) at a site with an excellent pace map, adjacent to the His bundle electrogram recording site. At that site, the sequence of the ventricular electrogram and late potential recorded during sinus rhythm reversed during spontaneous premature ventricular contractions with the same QRS morphology as the VT. This case shows that VT can arise from the LV ostium adjacent to the membranous septum. (PACE 2010; 33:e114–e118)